There it was, in all its glory - black, coarse, curly as a bedspring, coiling up from the velvety pad of my infant mons pubis. Back to that first little baby pube.Īge 2: “I was an athletic phenom at this age because I was so much bigger and stronger than everyone else. How much of that life would have been different if I’d cast off the very thing that had made me me? Then again, could I watch as my son suffered, knowing I could have saved him from that suffering? I didn’t know.
Yes, my childhood had been unusually challenging, but I was now 34 years old and, by most metrics, I had a great life. My body would be the final destination of the disease that had defined my family for generations. If one of our embryos tested positive for a mutation of the LHCGR gene, we could eliminate it. We learned that we could biopsy the embryos to find out if any of them carried the mutant LHCGR gene: the mutant responsible for a childhood rife with shame, embarrassment, and bullying the mutant responsible for my violent, antisocial behavior as a boy the mutant responsible for the troubled adolescence that my father, grandfather, great-grandfather, and I all endured, an adolescence that nearly delivered each of us to jail or worse. And then I was faced with the hardest decision of my life.
I came in a cup, my wife pumped her body full of hormones, scientists fertilized the eggs, and we ended up with five viable embryos. That is, until a little over four years ago, when my wife and I were trying to have a baby of our own, an endeavor that took two years and countless episodes of joyless appointment sex before we finally decided to do in vitro fertilization. This feeling of freakishness, of being strange and different, persisted well into adulthood, such that I refused to talk about it with anyone other than close friends and family. Being an anomaly for having pubes when you’re still breastfeeding isn’t typically something one brags about, which is why, like my forefathers, I spent the majority of my life hiding it, lying about it, repressing it, and avoiding it. Testotoxicosis affects fewer than one in a million men, and a leading expert estimates that we may only number in the hundreds. The result is premature everything: bone growth, muscle development, body hair, the full menu of dramatic physical changes that accompany puberty. The condition tricks the testicles into thinking the body is ready to go through puberty - so wham, the floodgates open and the body is saturated with testosterone. Having a mutant LHCGR gene leads to what doctors now call familial male-limited precocious puberty, an extremely rare disease that affects only men because you have to have testicles, which is why it’s also called testotoxicosis. But somewhere back in the lost recesses of my family’s genetic history, an unfortunate ancestor of mine was born with a mutant LHCGR gene. In women of reproductive age, the LHCGR triggers ovulation in men, it triggers testosterone production. On chromosome 2 in the DNA of all human beings, there’s a gene called the luteinizing hormone/choriogonadotropin receptor (LHCGR). We’ve all carried the same hereditary genetic mutation. It was the same for my father, and for his father, and for his father, and for the men in my family going back as far as we have records. There was no prelapsarian age of innocence for me I was born, I took a huge bite of the apple, and, by 2 years old, I was pretty much ready to get busy with Eve.
I have no recollection of a time before puberty, before the carnal cravings, the impulses, the angst and anger and violence. I couldn’t talk, I could barely walk, but I started growing a bush. I got my first pubic hair when I was 2 years old.